Functional amblyopia in kittens with unilateral exotropia

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Abstract
In two cats in which surgically induced, unilateral divergent strabismus had led to behaviourally determined amblyopia, a variety of electrophysiological parameters were determined in search of neuronal correlates of squint amblyopia. Tests that assess global neuronal excitability along the pathways from the two eyes to the visual cortex (areas 17 and 18) failed to reflect the functional inferiority of the squinting eye: retinographic responses and cortical evoked potentials elicited by Ganzfeld-stimulation and by stimulation of the optic nerves were identical for the two eyes. The ocular dominance distribution of neurons in area 17 showed the expected disruption of binocularity but failed to provide clear evidence for a functional inferiority of the squinting eye. At other levels of analysis, however, a clear difference between the two eyes was apparent: 1. Responses to optimally aligned light stimuli tended to be more sluggish and the under-representation of neurons with vertically oriented receptive fields was more pronounced in neurons driven from the deviated eye than in cells dominated by the normal one. 2. Interocular inhibition as assessed from electrically evoked potentials was found to be asymmetric; responses evoked from the amblyopic eye were suppressed more readily and over longer periods by conditioning shocks applied to the normal nerve than vice versa. 3. Numerous abnormalities reflecting the functional inferiority of the squinting eye became apparent in cortical potentials evoked by phase reversal of gratings of variable spatial frequency and contrast. A laminar analysis of these field potentials suggests impaired transmission along the intracortical pathways which relay activity to supragranular layers as a major cause for abnormal responses from the squinting eye. It is concluded that squint amblyopia is associated with a variety of neuronal changes at various levels of the visual system, the present data providing evidence for alterations at the cortical level.